Neurociruga
2007; 18: 420-422
Bilateral abducens nerve palsy following ruptured anterior communicating artery
aneurysm: report of 2 cases
E. Gksu; M. Akyz; D. Grkanlar and R. Tuncer
Department of Neurosurgery. Akdeniz University School of Medicine. Antalya. Turkey.
Summary
Isolated abducens nerve palsies associated with intra-
cranial aneurysms have rarely been reported. Their asso-
ciation with anterior communicating artery (ACoA) is even
rarer. Intracisternal clot formation and elevated intracranial
pressure has been proposed to be the responsible mecha-
nisms.
Herewith, we report two cases of bilateral abducens pal-
sies following ruptured ACoA aneurysms and speculated
the possible mechanisms.
Opening of Liliequist's membrane provides clinical
improvement due to CSF release.
KEY WORDS: Abducens nerve palsy. Liliequist's mem-
brane. Aneurysm.
Parlisis bilateral del nervio abductor despus de la
ruptura de un aneurisma de la arteria comunicante
anterior. Presentacin de dos casos
Resumen
Rara vez se ha publicado un caso de parlisis aislada
del nervio abductor craneal, asociada a un aneurisma. Su
asociacin con un aneurisma de la arteria comunicante
anterior (ACoA) es todava ms rara. Los mecanismos pro-
puestos son la formacin de un cogulo intracisternal y la
hipertensin intracraneal
Aportamos dos casos de parlisis bilateral del sexto par,
despus de la ruptura de aneurismas de la ACoA y discuti-
mos los mecanismos posibles.
La apertura de la membrana de Liliequist da lugar a una
mejora clnica , debido a la liberacin de l.c.r.
PALABRAS CLAVE: Parlisis nervio abductor. Aneu-
risma. Menbrana de Liliequist
Recibido: 13-10-06. Aceptado: 2-01-07
420
Introduction
Abducens nerve originates from pontomedullary junc-
tion. It crosses between anterior inferior cerebellary artery
(AICA) and labyrinthine artery and passes through the pre-
pontine cistern, Dorello's canal, cavernous sinus, superior
orbital fissure and orbita respectively. Due to its extremely
long extracerebral intracranial course the abducens nerve is
the most frequently involved cranial nerve in a number of
disorders3. About 10% of patients with sixth nerve paresis
have bilateral involvement2. Isolated abducens nerve pal-
sies associated with intracranial aneurysms have rarely
been reported. Their association with anterior communica-
ting artery (ACoA) is even rarer.
Cases
Case 1
A-51-year old woman was admitted with sudden onset
of headache, vomiting and diplopia. Neurologic examina-
tion showed bilateral sixth nerve palsy (Hunt-Hess grade
II). Computed tomography (CT) revealed subarachnoid
hemorrhage (Fischer grade II) (Figure l A). ACoA aneu-
rysm, determined with digital substraction angiography
(DSA) (Figure l B), was clipped succesfully on the sixth
day of her admission. Seven days after the operation her
left side abducens palsy recovered gradually and one
month later she had normal ocular movements.
Case 2
A-53-year old woman suffering from sudden headache,
nausea and temporary disturbance of consciousness was
admitted to our clinic. Bilateral abducens nerve palsies
were determined on neurologic examination (Hunt-Hess
grade II) (Figure 2 A, B). CT scan showed subarachnoid
and intraparanchymal hemorrhage located in basal cis-
terns, anterior interhemisferic fissure and right frontal lobe
(Fischer grade IV) (Figure 3 A) and cerebral angiograhy
revealed ACoA aneurysm (Figure 3 B). Microsurgical clip-
 Neurociruga
Bilateral abducens nerve palsy following ruptured anterior communicating artery aneurysm: report of 2 cases 2007; 18: 420-422

Figure 1. A: cranial CT
showing subarachnoid
hemorrhage Fisher Gra-
de II. B: Cerebral an-
giography revealing
ACoA aneurysm.

Figure 2. A, B: photograph of the patient showing bilateral abducens nevre palsy.

Figure 3. A: Cranial
CT showing subarach-
noid and intracisternal
hemorrhage and frontal
intracerebral hematoma
(Fisher Grade IV). B: ce-
rebral angiography re-
vealing ACoA aneurysm.

Figure 4. A, B: photograph of patient showing normal lateral ocular movements.

421

Gksu and col
ping of ACoA aneurysm was performed on the 15th day of
her admission. Postoperatively bilateral sixth nerve paresis
improved partially and one month later the neuroopthalmo-
logic examination was normal (Figure 4 A, B)
In both cases, Lillequist's membrane and prepontine
cistern were opened and meticulous cisternal toilette of the
subarachnoid clot was performed during the operation. In
the first case high pressure cerebrospinal fluid (CSF) drai-
nage was observed after opening the membrane.
Discussion
The frequency of abducens nerve palsies associated with
intracranial aneurysms is between 3.3% and 3.6%1,4. Isola-
ted or combined palsies of the sixth nerve had been reported
in various aneurysm localisations, including; infraclinoid
internal carotid, intracavernous carotid, anterior commu-
nicating, basilar, superior cerebellar, vertebral and poste-
rior inferior cerebellar arteries1,4,5,7. Several mechanisms
have been proposed to explain the bilateral involvement
of the abducens nerve after an aneurysm rupture such as:
direct compression of the aneurysm, elevated intracranial
pressure, vasospasm of the pontine branches of the basilar
artery affecting the abducens nuclei and direct compression
of the clot on the nerve in the prepontine cistern especially7.
Because of far way from the anterior communicating artery
the mechanism of bilateral sixth nerve involvement follo-
wing aneurysm rupture has been debated.
The inferior part of the carotid cistern and superior part
of the interpedincular cistern are in apposition - sometimes
causing a single membrane (Liliequist's membrane, 1959),
which may be thick or thin, but normally forming two sepa-
rate layers.
Following subarachnoid hemorrhage, this arachnoid
membrane may become thickened and create a loculation
of CSF in the interpedincular and prepontine area. Opening
of this membrane at operation almost always results in the
escape of some CSF, even in the profuse lumbar drainage6.
In the literature two cases of bilateral abducens palsies
following ruptured ACoA aneurysm had been reported. In
the first case, reported by Nathal et al. (1992) the mecha-
nism of the palsy was explained with the vasospasm of
the pontine branches of the basilar artery. and the deficits
had resolved completely three months after admission5. In
the second case, Ziyal et al. (2003) speculated that direct
compression of both abducens nerves was caused by the
extensive clot in the basal cisterns and bilateral palsies fully
recovered on the third postoperative day7.
In our first case both abducens nerves were probably
affected from the intracisternal entrapment of CSF. In our
second case the nerves were affected due to either the intra-
cisternal clot formation as Ziyal et al. speculated or high
intracranial pressure caused by the intracerebral hematoma
422
Neurociruga
2007; 18: 420-422
and SAH. In all mechanisms, the direct compression of the
nerve is the main cause. We cannot explain the mechanism
of the palsy with vasospasm of the pontine branches of the
basilar artery because there was neither clinical nor radio-
logical vasospasm.
We believe that the most important physiopathologic
mechanism of the bilateral sixth nerve palsies following
ACoA aneurysm rupture is the direct compression of the
nerve by blood or CSF. Recovery occurs usually 3-8 weeks
to literature1,5.
Conclusion
In this report, we speculated that bilateral sixth nerve
palsy can occur in the presence of intracisternal CSF entrap-
ment, clot formation and elevated intracranial pressure.
Opening of the Liliequist's membrane which provides CSF
release and extensive cisternal irrigation of the subarach-
noid clot, seems to be an effective surgical maneuver.
References
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Gilles, F.H.: Abducens length and vulnerability. Neurology
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4. Laun, A., Tonn, J.C.: Cranial nerve lesions following
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Willis. Neurosurg Rev 1988; 11: 137-141.
5 Nathal, E., Yasui, N., Suzuki, A., Hadeishi, H.: Ruptured
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Gksu, E.; Akyz, M.; Grkanlar, D.; Tuncer, R.: Bilateral
abducens nerve palsy following ruptured anterior commu-
nicating artery aneurysm: report of 2 cases. Neurociruga
2007; 18: 420-422.
Corresponding author: Ethem G iksu, M.D. Department of Neuro-
surgery. Akdeniz University School of Medicine, 07070, Antalya,
Turkey